scholarly journals The in Vivo Effect of Cordyceps sinensis Mycelium on Plasma Corticosterone Level in Male Mouse

2005 ◽  
Vol 28 (9) ◽  
pp. 1722-1725 ◽  
Author(s):  
Sew-Fen Leu ◽  
Chi-Hsien Chien ◽  
Chi-Yu Tseng ◽  
Yu-Ming Kuo ◽  
Bu-Miin Huang
1963 ◽  
Vol 41 (1) ◽  
pp. 1771-1777
Author(s):  
E. Stark ◽  
J. Fachet ◽  
Katherine Mihály

Prolonged exposure to ACTH considerably increased adrenal responsiveness in the rat both in vivo and in vitro. The last of 5 and 14 daily injections each produced a significantly higher blood corticosterone level than did a single injection. In the presence of ACTH added in vitro, adrenal corticosterone production in animals subjected to prolonged treatment with ACTH significantly exceeded the production per unit of weight and unit of time measured in saline-treated animals. Reduced adrenal responsiveness in the stage of resistance, elicited by formalin as a non-specific stress, cannot be invoked as an explanation for the absence of an increase in corticosterone secretion. The conclusion is that after prolonged exposure to non-specific stress there is no longer any ACTH hypersecretion.Twenty-four hours after the last injection of prolonged ACTH treatment there was inhibition of endogenous ACTH release by the pituitary gland, formalin produced no rise in the corticosterone level of the peripheral blood, and operative trauma caused substantially less ascorbic acid depletion than it did in saline-treated controls, although the plasma corticosterone level was normal or below normal.


1963 ◽  
Vol 41 (8) ◽  
pp. 1771-1777 ◽  
Author(s):  
E. Stark ◽  
J. Fachet ◽  
Katherine Mihály

Prolonged exposure to ACTH considerably increased adrenal responsiveness in the rat both in vivo and in vitro. The last of 5 and 14 daily injections each produced a significantly higher blood corticosterone level than did a single injection. In the presence of ACTH added in vitro, adrenal corticosterone production in animals subjected to prolonged treatment with ACTH significantly exceeded the production per unit of weight and unit of time measured in saline-treated animals. Reduced adrenal responsiveness in the stage of resistance, elicited by formalin as a non-specific stress, cannot be invoked as an explanation for the absence of an increase in corticosterone secretion. The conclusion is that after prolonged exposure to non-specific stress there is no longer any ACTH hypersecretion.Twenty-four hours after the last injection of prolonged ACTH treatment there was inhibition of endogenous ACTH release by the pituitary gland, formalin produced no rise in the corticosterone level of the peripheral blood, and operative trauma caused substantially less ascorbic acid depletion than it did in saline-treated controls, although the plasma corticosterone level was normal or below normal.


Author(s):  
Senthil Murugan Murugaiyan ◽  
Rajesh Bhargavan

AbstractObjectivesAluminium is present in food preparations, antacids and many medications. It causes neurodegeneration thereby resulting in a spectrum of neurological disorders such as dementia, Alzheimer’s disease and anxiety. Bacopa monnieri (BM) is widely used in ayurvedic medicine to improve memory functions. Its anxiolytic property was investigated in this study by using elevated plus maze (EPM) and plasma corticosterone level.MethodsThirty rats were assigned into five groups. Control group received distilled water, and 0.5% tween 80, AlCl3 group received Aluminium Chloride (AlCl3), Protective groups (BM100 + AlCl3 group and BM200 + AlCl3 group) received AlCl3 and BM at two different doses, and the BM200 group received BM. The EPM experiment was performed at the end of the 4th week of oral administration of BM and AlCl3 followed by the measurement of plasma corticosterone.ResultsOral administration of AlCl3 to rats increases the levels of anxiety as seen in a decrease in the percentage of entries into the open arms of EPM, an increase in grooming frequency and defecation index. However, the rats in the protective groups shown an increase in the percentage of open arm entries and rearing frequency, and decreased grooming frequency and defecation index. AlCl3 alone treated group showed a significant increase in the plasma corticosterone levels compared to the control group. Whereas the protective groups have shown a significant decrease in the plasma corticosterone levels than the AlCl3 alone treated group.ConclusionsHence the BM has potential role in reverting the anxiogenic effect of AlCl3 in the amygdala as it is evident from the plasma corticosterone levels and the EPM parameters of different groups under study.


1988 ◽  
Vol 66 (8) ◽  
pp. 1139-1143 ◽  
Author(s):  
Gary B. Glavin ◽  
Lorne J. Brandes

N,N-Diethyl-2-[4-(phenylmethyl)-phenoxy]-ethanamine hydrochloride (DPPE) is a para-diphenylmethane derivative that binds selectively and with high affinity to the microsomal antiestrogen binding site (AEBS). Recent studies with DPPE indicate that AEBS is closely related to a lower affinity non-H1, non-H2 histamine site that may be associated with calcium channels; the DPPE–AEBS site is different from that which verapamil binds, however. DPPE, but not verapamil, demonstrates antiproliferative effects in vitro and is antiestrogenic in vivo. We now show that DPPE profoundly inhibits restraint and cold stress and ethanol-induced gastric ulcer formation, accelerates ulcer healing, attenuates the stress-induced rise in plasma corticosterone level, and significantly reduces basal and H2 agonist (dimaprit)-stimulated and, to a lesser extent, bethanechol-stimulated gastric acid output in conscious rats. A nonulcerogenic but prostaglandin-depleting dose of indomethacin completely blocks the inhibitory effects of DPPE on stress ulcer formation. Conversely, verapamil only slightly attenuates dimaprit-stimulated gastric acid secretion and exacerbates ethanol-induced gastric ulcers; its anti-stress ulcer effects are only partially attenuated by indomethacin. These findings support the likelihood that the site of action of DPPE is different from that of verapamil, and that an effect on prostaglandins may, at least in part, contribute to its antiulcer and apparent cytoprotective effects.


Life Sciences ◽  
2004 ◽  
Vol 75 (9) ◽  
pp. 1051-1062 ◽  
Author(s):  
Yuan-Li Huang ◽  
Sew-Fen Leu ◽  
Bi-Ching Liu ◽  
Chia-Chin Sheu ◽  
Bu-Miin Huang

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Irina P. Butkevich ◽  
Viktor A. Mikhailenko ◽  
Tat'yana R. Bagaeva ◽  
Elena A. Vershinina ◽  
Anna Maria Aloisi ◽  
...  

Our researches have shown that gestational stress causes exacerbation of inflammatory pain in the offspring; the maternal 5-HT1A agonist buspirone before the stress prevents the adverse effect. The serotonergic system and hypothalamo-pituitary-adrenal (HPA) axis are closely interrelated. However, interrelations between inflammatory pain and the HPA axis during the hyporeactive period of the latter have not been studied. The present research demonstrates that formalin-induced pain causes a gradual and prolonged increase in plasma corticosterone level in 7-day-old male rats; twenty-four hours after injection of formalin, the basal corticosterone level still exceeds the initial basal corticosterone value. Chronic treatments of rat dams with buspirone before restraint stress during gestation normalize in the offspring pain-like behavior and induce during the acute phase in the formalin test the stronger corticosterone increase as compared to the stress hormonal elevation in animals with other prenatal treatments. Negative correlation between plasma corticosterone level and the number of flexes+shakes is revealed in buspirone+stress rats. The new data enhance the idea about relativity of the HPA axis hyporeactive period and suggest that maternal buspirone prior to stress during gestation may enhance an adaptive mechanism of the inflammatory nociceptive system in the infant male offspring through activation of the HPA axis peripheral link.


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